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par2 activating matriptase  (R&D Systems)


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    Structured Review

    R&D Systems par2 activating matriptase
    Colonic <t>PAR2</t> activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, <t>protease-activated</t> <t>receptor</t> <t>2;</t> PKA, protein kinase A; PKC, protein kinase C.
    Par2 Activating Matriptase, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+human+matriptase/Recombinant+Human+Matriptase%2FST14+Catalytic+Domain%2C+CF/pmc13098787-140-26-30
    Average 95 stars, based on 30 article reviews
    par2 activating matriptase - by Bioz Stars, 2026-11
    95/100 stars

    Images

    1) Product Images from "Monoclonal antibody inhibition of PAR2 reduces phenotype severity and pain in murine inflammatory bowel disease"

    Article Title: Monoclonal antibody inhibition of PAR2 reduces phenotype severity and pain in murine inflammatory bowel disease

    Journal: Pain Reports

    doi: 10.1097/PR9.0000000000001446

    Colonic PAR2 activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.
    Figure Legend Snippet: Colonic PAR2 activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Techniques Used: Activation Assay, Negative Control

    PAR2 activation in the colon by 2F sensitizes LSN responses to mechanical and chemical stimulation of the colon via endosomal internalization, PKA and PKC. LSN action potential firing after mechanical distention: gradually increasing intraluminal pressure from 0 to 80 mm Hg, and chemical application: 1 mM cinnamaldehyde and 1 µM capsaicin are illustrated in (A). (B) Responses to distention were quantified through the change in firing rate over increasing discrete pressure values. (C and D) Responses to chemical stimuli were quantified through the change in firing rate over time after application (vertical dotted line). 100 µM 2F stimulation, but not vehicle control, elicited sensitization of the LSN to (B) distention, (C) cinnamaldehyde, and (D) capsaicin. Pretreatment with PS2 before 2F stimulation reduced subsequent LSN responses to distention, cinnamaldehyde, and capsaicin compared with PN2. Pretreatment with H-89 and GFX, applied either simultaneously or individually, also reduced subsequent peak LSN responses to distention, cinnamaldehyde, and capsaicin compared with DMSO vehicle. (B–D) Independent samples t tests and one-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–9). * P < 0.05, ** P < 0.01, **** P < 0.0001. Data are presented as means ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.
    Figure Legend Snippet: PAR2 activation in the colon by 2F sensitizes LSN responses to mechanical and chemical stimulation of the colon via endosomal internalization, PKA and PKC. LSN action potential firing after mechanical distention: gradually increasing intraluminal pressure from 0 to 80 mm Hg, and chemical application: 1 mM cinnamaldehyde and 1 µM capsaicin are illustrated in (A). (B) Responses to distention were quantified through the change in firing rate over increasing discrete pressure values. (C and D) Responses to chemical stimuli were quantified through the change in firing rate over time after application (vertical dotted line). 100 µM 2F stimulation, but not vehicle control, elicited sensitization of the LSN to (B) distention, (C) cinnamaldehyde, and (D) capsaicin. Pretreatment with PS2 before 2F stimulation reduced subsequent LSN responses to distention, cinnamaldehyde, and capsaicin compared with PN2. Pretreatment with H-89 and GFX, applied either simultaneously or individually, also reduced subsequent peak LSN responses to distention, cinnamaldehyde, and capsaicin compared with DMSO vehicle. (B–D) Independent samples t tests and one-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–9). * P < 0.05, ** P < 0.01, **** P < 0.0001. Data are presented as means ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Techniques Used: Activation Assay, Control

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    Purification:

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    Article Snippet: Factor XIIa (FXIIa) is a promising target for developing new drugs that prevent thrombosis without causing bleeding complications.. A native cyclotide (MCoTI-II) is gaining interest for engineering FXIIatargeted anticoagulants as this peptide inhibits FXIIa but not other coagulation proteases.. Here, we engineered the native biosynthetic cyclization loop of MCoTI-II (loop 6) to generate improved FXIIa inhibitors.

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    Clinical Proteomics:

    Article Title: Engineering the Cyclization Loop of MCoTI-II Generates Targeted Cyclotides that Potently Inhibit Factor XIIa.
    Article Snippet: Factor XIIa (FXIIa) is a promising target for developing new drugs that prevent thrombosis without causing bleeding complications.. A native cyclotide (MCoTI-II) is gaining interest for engineering FXIIatargeted anticoagulants as this peptide inhibits FXIIa but not other coagulation proteases.. Here, we engineered the native biosynthetic cyclization loop of MCoTI-II (loop 6) to generate improved FXIIa inhibitors.

    Recombinant:

    Article Title: Engineering the Cyclization Loop of MCoTI-II Generates Targeted Cyclotides that Potently Inhibit Factor XIIa.
    Article Snippet: Factor XIIa (FXIIa) is a promising target for developing new drugs that prevent thrombosis without causing bleeding complications.. A native cyclotide (MCoTI-II) is gaining interest for engineering FXIIatargeted anticoagulants as this peptide inhibits FXIIa but not other coagulation proteases.. Here, we engineered the native biosynthetic cyclization loop of MCoTI-II (loop 6) to generate improved FXIIa inhibitors.

    Article Title: Autophagy of Candida albicans cells after the action of earthworm Venetin-1 nanoparticle with protease inhibitor activity
    Article Snippet: Recombinant bovine trypsin was purchased from Sigma-Aldrich (Germany) and chymotrypsin was provided by Bachem (Germany). .. Recombinant human matriptase-1/ST14 catalytic domain was purchased from R&D Systems (USA). .. Recombinant human matriptase-2 was obtained from Enzo Life Sciences (Switzerland).

    Article Title: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine.
    Article Snippet: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine Caroline M. Kopruszinski, John E. Linley, Peter Thornton, Alison S. Walker, Philip Newton, Sadhana Podichetty, Radhey Hemendra Ruparel, Luiz Henrique Moreira de Souza, Edita Navratilova, Guy Meno-Tetang, Ian Gurrell, David W. Dodick, Claire Dobson, Tharani Chessell, Frank Porreca and Iain Chessell

    Article Title: Inducible monovalent antigen binding protein
    Article Snippet: Purified plasmid DNA was transfected into Expi293 cells in accordance with Expi293 Expression System Kit (ThermoFisher) protocols, and maintained for 4-6 days post transfection. .. Purified exemplary monovalent antibodies were either proteolytically activated with 40 nM recombinant human matriptase (R&D Systems) in phosphate-buffered saline (PBS) or untreated control with PBS alone for overnight at room temperature. ..

    Article Title: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine
    Article Snippet: Thrombin from human plasma (Sigma) was used to activate PAR1 where detailed and diluted in PBS + 0.1% BSA to generate a 10 μM stock solution prior to final dilution in assay buffer. .. Recombinant human matriptase (R&D Systems) was diluted in 50 mM Tris-HCl plus 10% glycerol at a concentration of 23 μM prior to final dilution in assay buffer. ..

    other:

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    Article Snippet: All measurements were performed using a Fluostar Omega microplate reader (BMG Labtech, Germany) and 96-well black plates (BRAND, Germany).

    Concentration Assay:

    Article Title: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine.
    Article Snippet: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine Caroline M. Kopruszinski, John E. Linley, Peter Thornton, Alison S. Walker, Philip Newton, Sadhana Podichetty, Radhey Hemendra Ruparel, Luiz Henrique Moreira de Souza, Edita Navratilova, Guy Meno-Tetang, Ian Gurrell, David W. Dodick, Claire Dobson, Tharani Chessell, Frank Porreca and Iain Chessell

    Article Title: Efficacy of MEDI0618, a pH-dependent monoclonal antibody targeting PAR2, in preclinical models of migraine
    Article Snippet: Thrombin from human plasma (Sigma) was used to activate PAR1 where detailed and diluted in PBS + 0.1% BSA to generate a 10 μM stock solution prior to final dilution in assay buffer. .. Recombinant human matriptase (R&D Systems) was diluted in 50 mM Tris-HCl plus 10% glycerol at a concentration of 23 μM prior to final dilution in assay buffer. ..

    Saline:

    Article Title: Inducible monovalent antigen binding protein
    Article Snippet: Purified plasmid DNA was transfected into Expi293 cells in accordance with Expi293 Expression System Kit (ThermoFisher) protocols, and maintained for 4-6 days post transfection. .. Purified exemplary monovalent antibodies were either proteolytically activated with 40 nM recombinant human matriptase (R&D Systems) in phosphate-buffered saline (PBS) or untreated control with PBS alone for overnight at room temperature. ..

    Control:

    Article Title: Inducible monovalent antigen binding protein
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    Colonic <t>PAR2</t> activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, <t>protease-activated</t> <t>receptor</t> <t>2;</t> PKA, protein kinase A; PKC, protein kinase C.
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    Image Search Results


    Colonic PAR2 activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Journal: Pain Reports

    Article Title: Monoclonal antibody inhibition of PAR2 reduces phenotype severity and pain in murine inflammatory bowel disease

    doi: 10.1097/PR9.0000000000001446

    Figure Lengend Snippet: Colonic PAR2 activation by 2F elicits LSN responses that are mediated by endosomal internalization, PKA and PKC. (A) Experimental framework for LSN recordings showing a cannulated colon in a recording chamber with the LSN aspirated into a suction electrode. (B) Representative action potentials recorded from LSN afferent fiber prestimulation. (C and D) 100 µM 2F application elicits LSN responses illustrated by (C) action potential traces prestimulation and 15 minutes poststimulation and (D) change in LSN firing rate over time after stimulation via the luminal inflow (vertical dotted line). 2F-stimulation increased LSN firing (E and F). Timeline and peak change in firing rate after 100 µM 2F application (vertical dotted line) in tissue pretreated with (E) 50 µM PitStop2 (PS2) inhibitor for endosomal internalization or negative control PitNot2 (PN2) and (F) 100 µM H-89 dihydrochloride (H-89) and bisindolylmaleimide (GFX), PKA and PKC inhibitors or DMSO vehicle. (E) PS2 as well as separate and simultaneous pretreatment with H-89 and GFX reduced the peak response to 2F. (D and E) Independent samples t test comparing the peak change in firing rate (N = 5–9). (F) One-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–6). * P < 0.05, ** P < 0.01, *** P < 0.001 **** P < 0.0001. Data are presented as mean ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Article Snippet: When measuring the inhibitory concentration 50 (IC50), cells received PAR650097 mIgG or hIgG or isotype control antibodies, for 60 minutes at room temperature before addition of PAR2 activating matriptase (3946-SEB-010, R&D Systems, Abingdon, United Kingdom).

    Techniques: Activation Assay, Negative Control

    PAR2 activation in the colon by 2F sensitizes LSN responses to mechanical and chemical stimulation of the colon via endosomal internalization, PKA and PKC. LSN action potential firing after mechanical distention: gradually increasing intraluminal pressure from 0 to 80 mm Hg, and chemical application: 1 mM cinnamaldehyde and 1 µM capsaicin are illustrated in (A). (B) Responses to distention were quantified through the change in firing rate over increasing discrete pressure values. (C and D) Responses to chemical stimuli were quantified through the change in firing rate over time after application (vertical dotted line). 100 µM 2F stimulation, but not vehicle control, elicited sensitization of the LSN to (B) distention, (C) cinnamaldehyde, and (D) capsaicin. Pretreatment with PS2 before 2F stimulation reduced subsequent LSN responses to distention, cinnamaldehyde, and capsaicin compared with PN2. Pretreatment with H-89 and GFX, applied either simultaneously or individually, also reduced subsequent peak LSN responses to distention, cinnamaldehyde, and capsaicin compared with DMSO vehicle. (B–D) Independent samples t tests and one-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–9). * P < 0.05, ** P < 0.01, **** P < 0.0001. Data are presented as means ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Journal: Pain Reports

    Article Title: Monoclonal antibody inhibition of PAR2 reduces phenotype severity and pain in murine inflammatory bowel disease

    doi: 10.1097/PR9.0000000000001446

    Figure Lengend Snippet: PAR2 activation in the colon by 2F sensitizes LSN responses to mechanical and chemical stimulation of the colon via endosomal internalization, PKA and PKC. LSN action potential firing after mechanical distention: gradually increasing intraluminal pressure from 0 to 80 mm Hg, and chemical application: 1 mM cinnamaldehyde and 1 µM capsaicin are illustrated in (A). (B) Responses to distention were quantified through the change in firing rate over increasing discrete pressure values. (C and D) Responses to chemical stimuli were quantified through the change in firing rate over time after application (vertical dotted line). 100 µM 2F stimulation, but not vehicle control, elicited sensitization of the LSN to (B) distention, (C) cinnamaldehyde, and (D) capsaicin. Pretreatment with PS2 before 2F stimulation reduced subsequent LSN responses to distention, cinnamaldehyde, and capsaicin compared with PN2. Pretreatment with H-89 and GFX, applied either simultaneously or individually, also reduced subsequent peak LSN responses to distention, cinnamaldehyde, and capsaicin compared with DMSO vehicle. (B–D) Independent samples t tests and one-way ANOVA with post-hoc FDR-corrected independent samples t test (N = 5–9). * P < 0.05, ** P < 0.01, **** P < 0.0001. Data are presented as means ± SD. LSN, lumbar splanchnic nerve; PAR2, protease-activated receptor 2; PKA, protein kinase A; PKC, protein kinase C.

    Article Snippet: When measuring the inhibitory concentration 50 (IC50), cells received PAR650097 mIgG or hIgG or isotype control antibodies, for 60 minutes at room temperature before addition of PAR2 activating matriptase (3946-SEB-010, R&D Systems, Abingdon, United Kingdom).

    Techniques: Activation Assay, Control

    Structures of the masking reagent consist of: 1) a maleimide for conjugation, 2) a matriptase‐cleavable peptide (highlighted in purple), and 3) PEG to create steric hindrance, preventing the antibody from binding to the target.

    Journal: Chembiochem

    Article Title: Design and Characterization of Prodrugged Anti‐CTLA‐4 Antibodies

    doi: 10.1002/cbic.202500304

    Figure Lengend Snippet: Structures of the masking reagent consist of: 1) a maleimide for conjugation, 2) a matriptase‐cleavable peptide (highlighted in purple), and 3) PEG to create steric hindrance, preventing the antibody from binding to the target.

    Article Snippet: Prodrugged antibody was incubated with human matriptase (30:1 molar ratio, R&D system, 3946‐SE‐010) in 100 mM Tris buffer, pH7.6 at 37C.

    Techniques: Conjugation Assay, Binding Assay